Friday, August 13, 2021

A 60-something male presents with crushing chest pain

 I was reading ECGs on the system and saw this one:

What do you think?

I recognized this immediately as a variant due to some combination of Benign T-wave Inversion, Early repolarization, or LVH.  

1. There is ST Elevation in V2-V5

2. There is very high R-wave voltage in V4-V6

3. The leads with STE and T-wave inversion have very distinct J-waves.

4. The T-wave inversion is in leads V3-V6 (in contrast to Wellens', in which they are V2-V4)

5. There is high S-wave voltage in V2, with proportional ST elevation (consistent with LVH)

6. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves, or J-waves only

I was curious to see how the case presented, and it was managed by the treating physicians.  So I looked into it.  Here is the case:

This 60-something male presents with crushing left sided 10/10 chest pain.

The cath lab was activated.

Would you activate the cath lab?  I certainly would not blame you if you did.

But if you read this blog regularly, you too might recognize that this ECG is very likely to represent non-ischemic ST elevation and do a bit more digging into the chart.

Had you done more digging, you would have found that this patient frequently presents with chest pain, sometimes associated with cocaine use, and frequently also has elevated troponins (in the range of 80-100 ng/L, normal is less than 34 ng/L) and has multiple similar ECGs.

He had even had a negative angiogram just one month prior.

Here are 2 other ECGs within the last 6 weeks (both were initial ECGs on an ED presentation for chest pain):

5 weeks ago, with chest pain.

6 weeks ago, with chest pain:

Here is an echo from 10 days prior:

Normal left ventricular size, systolic function, and wall motion. The estimated left ventricular ejection fraction is 61%.

Left ventricular hypertrophy concentric moderate.


All ECGs without chest pain had the very similar morphology.


The angiogram was negative, just as it was one month prior.

Trops were 65, 74, 53, and 60.  (the patient has chronic myocardial injury, probably from LVH)

Learning Points:

1. MEMORIZE this morphology.

2. Patients with cocaine chest pain are not necessarily having any myocardial ischemia or vasospasm, though they might have it.

3. Patients with cocaine chest pain frequently have abnormal ECGs with non-ischemic ST Elevation.  Look for old ones and previous workups.

You can see more cases of "Benign T wave inversion" here:

Here is another case showing the combination of Benign T-wave Inversion and LVH:

This was a baseline ECG, not due to OMI

BTWI is a normal variant associated with early repolarization.  K. Wang studied it a while back.  He reviewed ECGs from all 11,424 patients who had at least one recorded during 2007 at Hennepin County Medical Center (where I work) and set aside the 101 cases of benign T-wave inversion.  97 were black.  3.7% of black men and  1% of black women had this finding.  1 of 5099 white patients had it.  Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group.

I have reviewed these 101 ECGs, and what strikes me is:

1. There is a relatively short QT interval (QTc < 425ms)  
2. The leads with T-wave inversion often have very distinct J-waves.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves). 
5. The leads with T-wave inversion (left precordial) usually have some ST elevation 
6. Right precordial leads often have ST elevation typical of classic early repolarization
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
9. II, III, and aVF also frequently have T-wave inversion. 

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